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Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The oxygen-binding properties of Hb molecule are unchanged in the third trimester of normal pregnancy and in pregnancy complicated by slight iron-deficiency anemia. Hb affinity to oxygen in whole blood is formed under the effect of the three main ligands H+, CO2, and 2,3-DPH. The development of hypocapnia in pregnant women results in elevation of pH values, reduction of pCO2, increase of intraerythrocytic 2,3-DPH concentration by 15-18%. Variously directed effects of H+, CO2, and 2,3-DPH on Hb affinity to O2 result in normal P50 values and therefore the Hb-O2 dissociation curve is not shifted to the right. Thus, in pregnant women with alkalosis 2,3-DPH effect on Hb affinity to oxygen completely eliminates H+ and CO2 effects but not compensates for Hb deficiency in the blood.
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PMID:[Status of the oxygen transport system of hemoglobin in physiological pregnancy and pregnancy complicated by iron deficiency anemia]. 147 17

In a five year period, 39 children (29 boys, 10 girls) aged 2 months to 13 years (mean 7.8 years) were studied who had suffered a major head injury (29 road traffic accidents, six falls, and four non-accidental injury). The injury had been assessed clinically and by cranial computed tomography or cranial ultrasound (in a single baby of 2 months). Initial Glasgow coma scores for all subjects ranged from 3-11 (mean 5.5), intact survivors 5-11 (7.4), minor handicap 4-11 (6.1), major handicap 3-6 (4.3), fatalities 3-6 (4.1). All were treated with sedation, paralysis, hyperventilation (arterial carbon dioxide tension 3.0-3.5 kPa), intracranial pressure monitoring and moderate body surface hypothermia to 32 degrees C. Nine children died and 30 survived (nine intact, 13 minor disability, and eight major disability). The worst cerebral perfusion pressure was over 40 mm Hg in all but one survivor, and less than 40 mm Hg in seven of nine fatalities. Severe hypocapnia both in the first 24 hours and overall was correlated with poor outcomes (dead or major disability), as were bilateral contusions or diffuse axonal injury.
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PMID:Management and outcome of severe head injuries in the Trent region 1985-90. 833 80

Forty adult patients with acute severe asthma were assessed for arterial blood gases and acid-base changes at presentation at the Casualty Unit, Kenyatta National Hospital, Nairobi, Kenya. Marked degrees of hypoxaemia (mean P(a)O2 of 8.02 kP(a)), hypocapnia (mean P(a)CO2 of 4.62kP(a)) with apparently normal pH (mean 7.384) were documented in the majority of these patients. Based on these findings, a significant number of the patients (68.5%) were either candidates (5.3%) or potential candidates (63.2%) for artificial ventilation. Records at this hospital suggest an increasing trend in asthma admissions and mortality. Additionally, Intensive Care Unit (ICU) admissions for asthma are associated with high mortality (54.4%). Pulsus paradoxicus emerged as the most significant (p = 0.002) clinical correlate to asthma severity. Central cyanosis was detected in none of the study patients suggesting that it is an unusual finding in the common presentation of acute severe asthma at this hospital. Its clinical detection would therefore imply an ominous clinical state. It is recommended that clinicians should take every opportunity to adequately assess their asthma patients before prescribing medications. They are also encouraged to more frequently request for blood gas studies in acute asthma. Those in charge of clinical teaching should direct appropriate efforts towards improved understanding of the pathophysiology and interpretation of acid-base disorders.
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PMID:Arterial blood gases and acid-base status of adult patients presenting with acute severe asthma at Kenyatta National Hospital, Nairobi. 150 18

Very low arterial CO2 tension (PaCO2) experienced by birds during high-altitude flight may result in cerebral vasoconstriction and reduced cerebral O2 delivery. To examine this possibility, we measured regional cerebral blood flow (CBF) and tissue PO2 in pentobarbital-anesthetized geese (Anser domesticus). Twenty-five-micrometer Teflon-coated platinum electrodes for H2-clearance measurements of local blood flow or tissue PO2 were implanted in the cerebral cortex in 11 geese. Tissue H2 and O2 were measured by voltage clamping the electrodes at +0.30 and -0.5 V, respectively. Washout kinetics of H2 gas administered via unidirectional lung ventilation was used to calculate local blood flow for those electrodes exhibiting one- or two-compartment washout kinetics of H2 (128 of 296 washouts in 31 electrodes). PaCO2 was controlled between 8 and 55 mmHg by altering pulmonary gas flow or by adjusting inspired PCO2. CBF decreased as PaCO2 fell from 50 to 20 mmHg but did not decrease further as PaCO2 was reduced below 20 mmHg. CBF was uniformly distributed in different regions of the cortex. Despite the plateau in CBF during severe hypocapnia, tissue PO2 continued to decline as PaCO2 fell below 20 mmHg. Severe alkalosis may limit cerebral O2 delivery in birds during high-altitude flight.
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PMID:Regional cerebral blood flow and tissue oxygenation during hypocarbia in geese. 151 Jan 62

Desflurane causes dose-dependent decreases in cerebrovascular resistance and cerebral metabolic rate of oxygen consumption (CMRO2), suggesting that desflurane is a cerebral arteriolar dilator with global flow-metabolism coupling similar to halothane and isoflurane. Desflurane is also similar to isoflurane in that cerebrovascular responsivity to carbon dioxide appears to be maintained. In the dog, arterial hypotension to 40 mm Hg induced with 2.4 MAC desflurane resulted in global decreases in cerebral blood flow of 60% and CMRO2 of 20%. Concentrations of cerebral metabolites of high-energy phosphates were not significantly deranged. The intracranial pressure data from humans are controversial. Desflurane and oxygen at 1 MAC caused sustained increases in cerebrospinal fluid pressure (maximum of 19 +/- 6 mm Hg) in patients undergoing craniotomy for mass lesion, despite prior establishment of hypocapnia. In a more recent study, the same investigators reported similar cerebrospinal fluid pressures before and after 0.5 MAC of either isoflurane or desflurane in 50% N2O. The electroencephalographic effects of desflurane are similar to those of isoflurane in humans, and burst suppression is easily achieved. There are no data available concerning possible interactions between desflurane and the outcome of a cerebral ischemic event. Similar to other potent volatile agents, desflurane can cause cerebral vasodilation and may result in intracranial pressure changes in vulnerable patients, but if adequate hyperventilation and depth of anesthesia are maintained, it is probably safe to use desflurane in a manner similar to isoflurane in patients with decreased intracranial compliance.
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PMID:Effects of desflurane on the central nervous system. 152 38

Carbon dioxide (CO2) has been well documented to act as a potent vasodilator of coronary vessels under normal conditions. But there is little data available on the effect of CO2 on the collateral perfusion of patients with coronary insufficiency. We studied the effects of CO2 on the myocardial tissue PO2 in anesthetized dogs with critical coronary stenosis. Twelve mongrel dogs were anesthetized with pentobarbital and ventilated with 100% O2 to maintain normocapnia. Electromagnetic blood flow (BF) probe was applied on the left anterior descending artery (LAD). Regional myocardial PO2 was measured at two different sites using two pairs of monopolar polarographic needle electrodes; one inserted in the epicardial (EPI) layer, and the other in the endocardial (ENDO) layer. These were placed in the regions supplied by LAD and circumflex. Following the baseline recording, critical stenosis of LAD was produced by adjusting a copper-wire clamp occluder until LADBF was reduced by 50%. After a stable normocapnic ventilation, hypocapnia was produced by hyperventilation. To induce hypercapnia, exogenous CO2 was added to the inspired gas stepwise until end-tidal CO2 fraction reached 10%. Hypocapnia resulted in a significant reduction in myocardial PO2 in both EPI and ENDO non-stenotic areas, while hypercapnia increased these PO2 values dose-dependently. After coronary stenosis, hypocapnia resulted in a small but significant reduction of PO2 in endocardial ischemic area. Hypercapnia did not induce any sign of reduced regional myocardial PO2 or evidence of regional or intramural "steal" phenomenon.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Effect of carbon dioxide (hypocapnia and hypercapnia) on regional myocardial tissue oxygen tension in dogs with coronary stenosis]. 155 62

We tested the hypothesis that altitude-induced hypocapnia in hens reduces eggshell conductance to water vapor (GH2O). Seven laying hens (Gallus domesticus) native to 1200 m were chronically exposed to high altitude (3800 m), and then to high altitude with sufficient inspired CO2 to relieve hypocapnia (3800 m + CO2). Egg GH2O was measured gravimetrically, shell thickness was measured with a micrometer, and aggregate pore area was calculated from measured values using Fick's law. Comparing results at 1200 m (n = 118) and 3800 m (n = 102), GH2O was reduced from 13.9 +/- 0.2 to 12.6 +/- 0.2 mg/(d.Torr)(mean +/- SE), shell thickness was reduced from 0.297 +/- 0.003 mm to 0.287 +/- 0.003 mm, and calculated aggregate pore area per egg was reduced from 1.97 +/- 0.03 mm2 to 1.72 +/- 0.03 mm2. When hypocapnia was relieved at 3800 m + CO2 (n = 82), GH2O was reduced even further to 11.1 +/- 0.2 mg/(d.Torr), shell thickness increased to 0.305 +/- 0.003 mm, and aggregate pore area was reduced to 1.61 +/- 0.03 mm2. Based on these results we reject our hypothesis. We conclude that hypocapnia is responsible for thin eggshells at altitude. Other physiological stimuli must cause the reductions in eggshell GH2O and pore area.
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PMID:CO2 and avian eggshell formation at high altitude. 155 44

Rings of canine bronchi were studied in vitro to determine the effects of halothane on the responses of airway smooth muscle to hypercapnia and hypocapnia. Bronchi were first contracted to 50% of maximal active force with acetylcholine (ACh), 5-hydroxytryptamine (5HT), potassium chloride (KCl), or the muscarinic agonist McN-A-343 (McN). The CO2 concentration of the bathing solution was then changed from 6% to either 1% (hypocapnia) or 10% (hypercapnia). In the absence of halothane, changes in CO2 concentration had no significant effect on muscles contracted with ACh. With all other contractile agonists, increasing the CO2 concentration caused bronchial relaxation, while decreasing the CO2 concentration caused contraction. In the presence of 2 MAC halothane, hypocapnia relaxed bronchi contracted with the muscarinic agonists ACh or McN; the responses to hypocapnia of bronchi contracted with KCl and 5HT were not significantly changed by halothane. Halothane had no effect on the responses of the bronchi to hypercapnia. We conclude that airway smooth muscle contracted with cholinergic agonist relaxes in response to hypocapnia when exposed to 2 MAC halothane; this mechanism may contribute to the depression of hypocapnic bronchoconstriction caused by halothane in vivo.
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PMID:Halothane alters the response of isolated airway smooth muscle to carbon dioxide. 156 97

Although hyperventilation with hypocapnia is frequently used in the management of neurosurgical patients in whom sensory-evoked potentials may be monitored, the effects of hypocapnia on evoked potentials have not been described with precision. In the present experiment, the effects of randomized arterial carbon dioxide tensions of 20, 25, 30, and 35 mm Hg on spinal, subcortical, and cortical somatosensory-evoked potentials (SEPs) were measured in dogs anesthetized with 1.40% isoflurane. Other variables known to affect the SEP (temperature, blood pressure, and arterial oxygen tension) were stable throughout the experiment. Hypocapnia caused reductions in the latencies of the early peaks of the spinal and subcortical SEPs. These differences were small, consisting of a 2% shortening of latency at 20 mm Hg carbon dioxide tension when compared with 35 mm Hg. No changes were detected in the later subcortical and cortical latencies. SEP amplitudes were also unchanged. These results in a controlled animal study corroborate the direction and magnitude of changes due to hypocapnia observed by other investigators in surgical patients. The magnitude of the changes indicates that SEP monitoring sensitivity is not compromised by clinically useful levels of induced hypocapnia during isoflurane anesthesia. Because hypocapnia may produce small SEP changes, baseline recordings should be acquired prior to initiation of hyperventilation. It is not warranted, however, to impute a severe deterioration of the SEP to hypocapnia alone, and causes must be sought elsewhere in a patient's status and management.
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PMID:Effects of hypocapnia on canine spinal, subcortical, and cortical somatosensory-evoked potentials during isoflurane anesthesia. 158 48

Alterations in arterial oxygen and carbon dioxide influence cerebrovascular resistance and therefore cerebral blood flow (CBF), but the magnitude of these CBF responses have not been well defined in normal humans. Duplex scanning (B-mode imaging and pulsed Doppler shift analysis) was used to measure internal carotid blood flow (ICBF) as an indicator of CBF in 20 normal subjects during alterations of arterial O2 and CO2. End-tidal PCO2 (PETCO2) was measured by mass spectrometry, arterial oxygen saturation by pulse oximetry, and unilateral (right) ICBF by duplex scanning. A variety of gas mixtures were administered to achieve hypoxemia (FIO2 = 0.075-0.10) and hypercapnia (FICO2 = 0.05) or the subject was asked to hyperventilate to PETCO2 = 16-24 mm Hg. The ICBF was determined five times in each of six conditions: (1) normoxia/normocapnia; (2) normoxia/hypercapnia; (3) normoxia/hypocapnia; (4) hypoxia/normocapnia; (5) hypoxia/hypercapnia; and (6) hypoxia/hypocapnia. During normoxia and normocapnia, the mean ICBF was 330 +/- 19 (SEM) mL/min. Specific CO2 reactivity was 7.4 +/- 0.7 mL/min/mmHg, which is equivalent to 2.3% +/- 0.1% of normocapnic blood flow per mm Hg change in CO2. During normocapnia, ICBF increased by 2.9 +/- 0.9 mL/min for each percentage decrease in oxygen saturation. Using an ANOVA with repeated measures to fit the responses, the following statistically significant relationship was found: ICBF (mL/min) = 333 + 6.3.(PETCO2 - 40) + 2.7 DSO2 +/- 81 where DSO2 is arterial desaturation (100 - arterial saturation). An additional "between subject" variation had a mean of 0 and a standard deviation of 82 mL/min. There was no statistically significant evidence of an interaction between O2 and CO2 response. Our data suggest that hypoxia and carbon dioxide changes will alter CBF simultaneously and additively. Duplex scanning of the internal carotid artery, which can be performed at the bedside, is sufficiently sensitive to detect changes in ICBF and internal carotid artery oxygen delivery.
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PMID:Human cerebrovascular response to oxygen and carbon dioxide as determined by internal carotid artery duplex scanning. 158 51


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